256 Maternal Antibodies to Fetal Brain Neurons and Autism
the developing brain is illustrated by the effect of lipopolysaccharides on the
permeability of blood vessels in brain tissue at a critical stage of brain develop
ment, carried out in rats and opossums equivalent to weeks 22–28 gestation
in humans. In these experiments these blood vessels showed a leakage of
plasma proteins that were confirmed in postnatal animals.
In a clinical setting if a mother develops an infection, the fetus may be born
prematurely and in some cases brain injury has been detected with the devel
opment of cerebral palsy. Leakage of proteins from plasma into white matter in
the presence of maternal infection has been suggested to be part of the etiol
ogy. As elegantly reviewed by Saunders et al. [47], many other possibilities of
functionally important changes in influx or efflux mechanisms following a
pathological insult to the developing brain have rarely been considered.
In evolutionary terms, it is counterintuitive to believe that placental life
(viviparous) forms that give live birth and carry the placenta would be so suc
cessful if they did not co‐evolve parallel tools to protect their fetuses against
pathogens. In many circumstances, viviparity of various forms offers excellent
protection from microbial and viral infections and predators and permits
flexibility in adapting to unreliable weather and adverse circumstances.
The evidence presented would attest to the fact that very few adverse natural
circumstances can perturb the balance of life between a pregnant woman and
her offspring. It is certain that our ancestors and early humans were exposed
to a much greater number and variety of infections agents than we are today.
So, why are ASD and the other myriad of neurodevelopmental and neuropsy
chiatric disorders increasing at such a high rate? We believe that manmade
chemicals are hurting human life on earth.Summary and Conclusions
Maternal antibodies directed against fetal brain antigens are detected in ASD
by numerous researchers in a subset of mothers of children with ASD. Further,
there is now an abundance of evidence supporting their deleterious role in
neurodevelopment. For the most part, these studies have described similar
experimental outcomes, and given the clinical and biological heterogeneity of
ASD, there likely exists a complex relationship between the presence of mater
nal neuroantibodies and the developmental course of exposed offspring. It is
still unclear how and when these maternal neuroantibodies arise in the mater
nal blood and what factors permit the leakage of neuroantigens from a fetal
brain into the maternal circulation.
We have provided detailed analyses of the mechanism underlying the
origins of fetal neuroantigens and the maternal origins of neuroantibodies–
autoantibodies, which cannot be generalized as causes of other neuro
developmental and neuropsychiatric disorders. However, we believe that